scott@vtx-cpd.com
Forum Replies Created
-
AuthorPosts
-
Replying to Magda Upton 13/03/2023 - 14:39
Magda!
What a joy to have you here! Thank you so much for all of the support!
I really appreciate it! I really hope you enjoy the course.
Scott 🙂
Replying to gemma.ives@protexin.com 13/03/2023 - 14:36
Gemma!
Lovely to see you here! Thank you so much for all of the support!
I hope you enjoy the course!
Scott 🙂
Replying to Rachel F. 14/03/2023 - 17:28
Thanks for the update.
Would be good to get an update with progress. I am alwats surprised by these cases, often insulin requirement does not reduce that much.
Thank you again for all of your support.
Scott 🙂
Replying to Rachel A. 14/03/2023 - 14:34
Hey Rachel.
Great questions. I think we are right to be concerned about the over prescription of PPI’s and the effect on the microbiome. I think there is probably a place for their use with brachycephalic patients however.
We do have evidence that BOAS patients and some patients undergoing prolonged orthopaedic surgery can experience potentially significant gastro-oesophageal reflux (GOR). The use of omeprazole in these patients has also now been shown to help prevent the change in distal oesophageal pH that accompanies GOR, but this is probably as a result of the change in gastric pH that omeprazole mediates, not because omeprazole reduces the actual frequency of GOR. However, preventing acid damage to the distal oesophagus where there is a known risk is appropriate, so it is therefore rational to use omeprazole in some surgical patients where there is a risk of GOR, and especially in BOAS patients where GOR is a known risk.
These are some useful references:
Panti, A. et al. (2009). The effect of omeprazole on oesophageal pH in dogs during anaesthesia. J. Small Anim. Pract. 50, 540–544
Kaye, B. M., Rutherford, L., Perridge, D. J. & Ter Haar, G. (2018). Relationship between brachycephalic airway syndrome and gastrointestinal signs in three breeds of dog. J. Small Anim. Pract. 59, 670–673
Shaver, S. L. et al. (2017). Evaluation of gastroesophageal reflux in anesthetized dogs with brachycephalic syndrome. J. Am. Anim. Hosp. Assoc. 53, 24–31
In short, I would consider using pre GA using this protocol:
https://pubmed.ncbi.nlm.nih.gov/33769569/
Hope that helps.
Scott 🙂
Replying to Ornella R. 10/03/2023 - 13:13
Hey Ornella.
Sorry for the delay in getting back to you!
I would only use omeprazole in NSAID toxicity when there are signs of ulceration (melena or haematemesis) or there are prolonged GI signs. In actutre cases where we induce emesis and support, I would not routeninely use.
The antioxidants is interesting. This come from human medicine:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884640/
“The role of antioxidants, especially vitamins C and E, in the prevention of NSAID-induced gastric injury is relatively little studied, and large outcome studies are missing. Both vitamins C and E seem to play a role in the preservation of gastric mucosal integrity; vitamin C is actively secreted into the gastric lumen of healthy subjects, and its concentrations are decreased in patients with gastroduodenal diseases such as peptic ulcer disease, gastric malignancy, or H. pylori-associated gastritis. The underlying molecular mechanisms, however, are not fully understood.
We were recently able to show that the gastroprotective effects of vitamin C as observed in humans might – at least in part – be mediated by haeme-oxygenase-1 (HO-1). HO-1 is a ubiquitous and crucial tissue-protective enzyme with vasodilative, anti-inflammatory and antioxidant properties. In the stomach HO-1 might counteract the two major mechanisms of NSAID-induced gastric injury: disturbance of gastric microcirculation and free radical release. The mechanisms of HO-1 induction seem to be cell-type specific; a nonstressful induction was recently postulated as a therapeutic target. We identified vitamin C as a potential nonstressful inducer of HO-1 in the stomach. However, to date there are only very limited data about this enzyme in the stomach. Guo et al. showed that healing of gastric ulcers in rats is paralleled by an upregulation of HO-1. Further studies are needed to examine the role of HO-1 in the stomach in vivo. Our recent findings, however, are in favour of the supplementation of vitamin C in order to prevent NSAID gastropathy – showing an impact beyond its sole antioxidant properties.”
As far as I am aware, there is no evidence for this in our patients.
Interesting though!
Scott 🙂
Replying to Samanta A. 14/03/2023 - 16:06
Hey Samanta.
This is a great question! I hope you enjoyed the recording.
I think this depends a bit on the cat and how tricky tableting is!
If can tablet them, then I go for at least 4 weeks, then taper and stop, but if had recurrent episodes have ad some on for months.
What is your experience?
Scott 🙂
Replying to Samanta A. 14/03/2023 - 16:13
Hello Samanta.
Lovely to hear from you. I hope you are well.
This is a great question. I think it depends on how the patient responds to the procedure. Is there concurrent hepatitis?
If there are persistently elevated liver enzymes, I would consider continuing the UDCA. Would there be an option to take a liver biopsy at the time?
UDCA has lots of other beneficial properties beyond the bile/GB effects:
“Ursodeoxycholic acid (UDCA) is a hydrophilic bile acid that is believed to have several beneficial properties: UDCA may displace more toxic hydrophobic bile acids from the circulating pool, it has a choleretic effect which increases the excretion of endogenous toxins in the bile, it has a cytoprotective effect by inhibiting hepatocyte apoptosis, and immunomodulatory effects, such as the suppression of interleukin-2 expression. It is the only Federal Drug Administration approved treatment for primary biliary cirrhosis in humans. When used at a dosage of 10-15 mg/kg PO q 24 h in dogs and cats, this drug has few side effects other than occasionally causing diarrhea. Because of its choleretic effect and the displacement of more toxic hydrophobic bile acids, there is a rationale behind using this drug in dogs and cats with intrahepatic and extrahepatic cholestasis, such as cholangitis in cats. In a recent retrospective study of cats with lymphocytic cholangitis, those treated with prednisolone survived longer than those treated with UDCA.34 However, this study does not prove that UDCA lacks efficacy for treating feline lymphocytic cholangitis as for ethical reasons treatment was not compared to a placebo. The use of UDCA in dogs and cats with complete bile duct obstruction is controversial as some clinicians are concerned about the possibility of it increasing the probability of gallbladder rupture. Other clinicians feel comfortable using UDCA in this situation and studies in rats where bile duct ligation was performed actually indicate that it has a beneficial effect on markers of oxidative stress and apoptosis. However, it is important to note that surgical intervention is indicated in most dogs or cats with complete bile duct obstruction. Where the patient has no or mild clinical signs, UDCA is sometimes used as part of the medical management of non-obstructed, canine gallbladder mucoceles. Furthermore, due to its purported immunomodulatory and antiapoptotic effects there is a theoretical reason to use UDCA in dogs with chronic hepatitis although its efficacy in this condition has not been critically evaluated.”
In short, I would keep using it if persistent liver enzyme increases!
Hope that helps.
Scott 🙂
Replying to Rachel F. 13/03/2023 - 19:58
Hey Rachel.
Thanks for the update. What did you decide to do treatment wise?
Scott 🙂
Replying to Rachel F. 13/03/2023 - 14:17
Hey!
Glad you enjoyed it. I will get Andy to have a look at this ASAP.
Scott 🙂
Replying to Sarah H. 12/03/2023 - 09:53
Sarah!
Lovely to have you here. Time flies when you are having fun I suppose!
Thanks for your kind words, that means a lot. I will indeed link to some more GI podcasts.
Francesco is such a lovely guy!
I really hope you enjoy the course.
Scott 🙂
Replying to Helen Bradley 22/02/2023 - 10:51
Hey again!
I also thought this review would be helpful:
https://drive.google.com/file/d/1TB3rf4UecB9qglDiBsYLYhDjBhQ2Why3/view?usp=share_link
Scott 🙂
Replying to Helen Bradley 22/02/2023 - 10:51
Hey Helen.
Sorry for the delay in getting back to you. I asked this question to one of our ECC specialists over on the ECC course and got the following back:
“So… yes I would use them in dogs with severe haemorrhagic diarrhoea/gastroenteritis a lot. I think I may be biased to the ones we see, so I am talking about the ones that come unwell with signs of hypovolaemic shock and severe dehydration/haemoconcentration. These ones typically come with high PCV and “normal” TS so for example 65%/60g/L, in these ones I know that if hypovolaemic I will need to fluid resuscitate so may end up needing 5-20mL/kg over a few boluses and then I will need high rates of IVFT to account for on going losses, rehydration and maintenance and when you calculate this sometimes is as high as 6-8mL/kg/h. There is two sides to this and one is that we know that actually the use of crystalloids itself will damage the glycocalyx and you will gave shedding and then this will lead to increased vascular permeability etc. and the second side to this is that when my PCV is normalised when the patient is rehydrated, say comes from 65 to 45%, I know my solids will ave tanked and probably be from 60 to 30-40g/L and at this stage this becomes a problem also with on going increased permeability, increased oncotic pressure etc. So that is why I tend to come in early with plasma to prevent this from happening, and when plasma is used as is a colloid… you can also allow yourself to use lower fluid rates so in the same example if you calculated you may need 6-8mL/kg/h if you combine plasma and crystalloids you may get away with 4-5mL/kg/h instead.
For the hypoalbuminaemic GI patients… I don’t think there is a number really. So if I think PLE that I have treated alongside medicine; these patients are different as stable so unless I had to fluid resuscitate or need IVFT I would not consider it, even if their albumin is really low. Now for a PLE patient who isn’t great and is now third spacing and say it has abdominal effusion, and that is increasing the abdominal pressure which is compromising the gut blood supply and they are not doing great. I tend to remove abdominal fluid really slowly over a few hours, then replace with plasma – and the times we have done this they tend to have really low alb on low teens.”
Hope that helps.
Scott 🙂
Replying to Rosie Marshall 08/03/2023 - 11:33
Hey Rosie.
Lovely to hear from you. I hope you are well.
So I never heard back from VPIS about this! I have spoken to several people about this topic, including a couple of ECC specialists.
For acute ingestion of ibuprofen managed symptomatically with emesis and IVFT I would not routinely use omeprazole prophylactically.
I would only use omeprazole in these cases when there are ongoing, severe GI signs or any evidence of melena or haematemesis.
What did you do with your case? Hope this helps.
Scott 🙂
Replying to Siriol B. 08/03/2023 - 18:32
Hello!
Great question. The idiopathic cases, most of them require lifelong management. The expectation would not be that oesophageal function would return. The aim of any medical management would be to reduce clinical signs as much as possible, but not a return to normal function.
Interesting comments regarding the feeding. Having a dog with a megaoesophagus is intense, and I have a lot of respect for owners.
Scott 🙂
Replying to Sybil Dryburgh 08/03/2023 - 18:57
HAHAHAH!
It is a tough read!
Scott 🙂
-
AuthorPosts